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ToxSci Advance Access originally published online on February 23, 2005
Toxicological Sciences 2005 85(1):507-514; doi:10.1093/toxsci/kfi128
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Toxicological Sciences vol. 85 no. 1 © The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

No Increase of Apoptosis in Regressing Mouse Liver after Withdrawal of Growth Stimuli or Food Restriction

Wilfried Bursch1, Ute Wastl, Karin Hufnagl and Rolf Schulte-Hermann

Medizinische Universität Wien, Univ. Klinik für Innere MedizinI, Abtl. Institut für Krebsforschung, Borschkegasse 8a, A-1090 Wien

Received July 20, 2004; accepted February 14, 2005

In short-term in vivo experiments, liver growth and regression in mice with high (C3H/He), intermediate (B6C3F1) or low (C57BL/6J) susceptibility to hepatocarcinogenesis was compared. Liver growth was induced by dietary administration of phenobarbital (PB; 750 ppm) or nafenopin (NAF; 500 ppm). PB or NAF treatment for 7 days produced moderate increases of liver DNA (15% or 25–28%, respectively) along with pronounced hypertrophy. Liver growth was strongest in C3H/He mice. Cessation of PB or NAF treatment led to a rapid regression of liver hypertrophy. However, the enhanced hepatic DNA content persisted for at least 2 weeks in all mouse strains. Apoptosis was not increased at any time after cessation of treatment in all strains. Food restriction to 60% of the ad libitum intake did not amplify either regression of liver hyperplasia or the occurrence of apoptosis. No strain difference in the occurrence of apoptosis was detected. Mouse hepatocytes in liver regressing after mitogen withdrawal do not enter apoptosis as readily as rat hepatocytes.

Key Words: phenobarbital; nafenopin; C3H/He; B6C3F1; C57Bl/6J; liver weight; protein content; DNA content; DNA synthesis; apoptosis.


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